The aim of the present project is to continue the evaluation of different approaches to myocardial preservation during ischemic arrest which has been an ongoing project for 2 years. Initial studies have documented the necessity for both cardioplegia and hypothermia to be used together to conserve myocardial function during ischemic arrest in the pig heart model. Comparing cardioplegic agents (magnesium-procaine vs. potassium) has shown no demonstrable difference in maintaining myocardial contractility following arrest. Continuing research will explore the relative efficacy of magnesium vs. potassium in maintaining high energy phosphate compounds during arrest and will study the relative value of adjunctive agents (procaine, mannitol, 6-methylprednisolone, glucose, and calcium) in preserving myocardial cellular integrity during and following cardioplegic arrest. The use of different cardioplegic carrier solutions will be studied to determine what role they play in myocardial preservation during cardioplegic arrest, and changes will be made in the initial reperfusion fluid following arrest to determine what constitutes an optimal medium for replenishing myocardial oxygen debt. Myocardial preservation will be evaluated: 1) by biochemical means: measuring myocardial cellular adenosine triphosphate, creatine phosphate, glycogen, and cellular creatine phosphokinase; 2) by measuring myocardial function using left ventricular dp/dt max and dp/dt/p (measurements of left ventricular myocardial contractility) and ventricular diastolic compliance; 3) by measuring left ventricular perfusion using the radioisotope microsphere technique for determining endocardial and epicardial flow and directly measuring total myocardial blood flow; and 4) by electron microscopic evaluation of left ventricular ultrastructure.